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Factors predicting an arrhythmogenic superior vena cava in atrial fibrillation ablation: Insight into the mechanism
Factors predicting an arrhythmogenic superior vena cava in atrial fibrillation ablation: Insight into the mechanism Shinsuke Miyazaki, MD, Hiroshi Taniguchi, MD, Shigeki Kusa, MD, Noboru Ichihara, MD, Hiroaki Nakamura, MD, Hitoshi Hachiya, MD, Yoshito Iesaka, MD, FHRS From the Cardiovascular Center, Tsuchiura Kyodo Hospital, Tsuchiura, Ibaraki, Japan. BACKGROUND The superior vena cava (SVC) is an infrequent but important source of atrial fibrillation (AF), but is not always easy to identify. OBJECTIVE This study aimed to identify predictors of an arrhythmogenic SVC (a-SVC) in patients undergoing AF ablation. METHODS Eight hundred thirty-six consecutive patients undergoing AF ablation were analyzed. All patients underwent pulmonary vein antrum isolation during the index procedure. An a-SVC, defined as SVC-triggered AF and an SVC associated with the maintenance of AF, was evaluated by mapping catheters throughout the procedure. RESULTS An a-SVC was identified in 44 patients (5.3%) during a total of 1063 procedures. Patients with an a-SVC were younger, less obese, and had a smaller left atrial (LA) size and more paroxysmal AF than those without an a-SVC. The presence of structural heart disease and hypertension was lower, and the coexistence of spontaneous common atrial flutter (AFL) before or during the index procedure was higher in those with an a-SVC than in those without. A multiple logistic regression analysis revealed that the LA size (odds ratio 0.93; 95% confidence interval 0.88–0.99; P ¼ .038) and coexistence of
Introduction Recognition and targeting of pulmonary vein (PV) triggers have led to a dramatic rise in the efficacy and prominence of atrial fibrillation (AF) catheter ablation.1–3 Despite the critical role of the PVs and PV antrum in AF,3–5 non-PV foci have also been established as important sources of AF.6 The superior vena cava (SVC), one of the thoracic veins, contains atrial muscle sleeves extending up to a short distance from the right atrium (RA)7 and acts not only as a trigger but also as a driver of AF like the PVs.8,9 Although electrical isolation has been the established strategy for arrhythmogenic SVCs,10 the identification is not always easy and missing the arrhythmogenicity leads to an arrhythmia recurrence after the ablation procedure. In fact, in some of the cases, the arrhythmogenicity is identified in a repeat procedure and various provocative maneuvers are required to Address reprint requests and correspondence: Dr Shinsuke Miyazaki, Cardiology Division, Cardiovascular Center, Tsuchiura Kyodo Hospital, 11-7 Manabeshin-machi, Tsuchiura, Ibaraki 300-0053, Japan. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
spontaneous common AFL (odds ratio 2.01; 95% confidence interval 1.00–4.02; P ¼ .048) were independent predictors identifying an aSVC. Although 19 patients (43.2%) required repeat procedures, 39 (88.6%) were free from any atrial tachyarrhythmias without antiarrhythmic drugs at a median of 16.5 months (25th–75th percentiles 9.0–27.0 months) after a mean of 1.5 ⫾ 0.7 procedures. CONCLUSION A smaller LA size and coexistence of spontaneous common AFL were independent predictors of an a-SVC in the context of AF ablation. KEYWORDS Superior vena cava; Arrhythmogenicity; fibrillation; Predictor; Catheter ablation
Atrial
ABBREVIATIONS AF ¼ atrial fibrillation; AFL ¼ atrial flutter; ATa ¼ atrial tachyarrhythmia; CTI ¼ cavotricuspid isthmus; ECG ¼ electrocardiogram/electrocardiographic; LA ¼ left atrium/atrial; PV ¼ pulmonary vein; PVAI ¼ pulmonary vein antrum isolation; RA ¼ right atrium; RF ¼ radiofrequency; SVC ¼ superior vena cava (Heart Rhythm 2014;11:1560–1566) I 2014 Heart Rhythm Society. All rights reserved.
find it out.11 Thus, knowing the predictors of arrhythmogenic SVCs would be helpful in the context of AF ablation. The objective of this study was to elucidate the predictors of arrhythmogenic SVCs (triggers and perpetuators of AF) in the context of AF ablation.
Methods Study population This study consisted of 836 consecutive patients who underwent catheter ablation of drug-resistant AF between April 2010 and December 2013 at our institute. The arrhythmogenicity of the SVC was evaluated with a mapping catheter throughout the ablation procedure in all procedures. All patients underwent pulmonary vein antrum isolation (PVAI) in the index procedure. An additional SVC isolation was undertaken for arrhythmogenic SVCs whenever the arrhythmogenicity was identified. An arrhythmogenic SVC was defined as an SVC triggering AF and an SVC associated with the maintenance of AF.9 Solitary premature atrial contractions without AF originating from the SVC did not define an arrhythmogenic SVC in this study. AF was http://dx.doi.org/10.1016/j.hrthm.2014.06.016
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classified according to the 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of AF. All patients gave their written informed consent for participation in the study.12
Mapping and ablation protocol All antiarrhythmic drugs were discontinued for at least 5 half-lives before the procedure. All patients were effectively anticoagulated for 41 month before the procedure. Transesophageal echocardiography was performed to exclude any atrial thrombi. The surface electrocardiogram (ECG) and bipolar intracardiac electrograms were continuously monitored and stored on a computer-based digital recording system (LabSystem PRO, Bard Electrophysiology, Lowell, MA). The bipolar electrograms were filtered from 30 to 500 Hz. A 7-F 14-pole 2-site mapping catheter (Irvine Biomedical Inc, Irvin, CA) or a 7-F 20-pole 3-site mapping catheter (BeeAT, Japan Life Line, Tokyo, Japan) was inserted through the right jugular vein. The proximal poles were positioned at the SVC-RA junction and distal poles in the coronary sinus for pacing, continuous recording, and internal AF cardioversion during the entire procedure. The proximal electrodes enabled continuous monitoring of the SVC during the entire procedure. The electrophysiology study was performed under mild sedation obtained with pentazocine and hydroxyzine pamoate.
Ablation procedure Ablation was performed according to the strategy described previously.13–15 In brief, after a single transseptal puncture, 2 long sheaths (SL0, St Jude Medical, Minneapolis, MN) were introduced into both superior PVs. Pulmonary venography during ventricular pacing and contrast esophagography were performed to obtain the relative locations of the PV ostia vis-à-vis esophagus. A 100 IU/kg body weight dose of heparin was administered after the transseptal puncture, and heparinized saline was also infused to maintain the activated clotting time at 250–350 seconds. Two circular mapping catheters (Lasso, Biosense Webster, Diamond Bar, CA) were placed in the superior and inferior PVs, and the left- and right-sided ipsilateral PVs were circumferentially and extensively ablated guided by a 3-dimensional mapping system (CARTO 3, Biosense Webster). Posteriorly, ablation was performed anatomically in the left atrium (LA), 1–3 cm from the PV ostia. Anteriorly, ablation was performed on the edge of the left PVs guided by the earliest PV potentials. The end point was achievement of bidirectional conduction block between the LA and PVs.16 Radiofrequency (RF) current was delivered point by point with a 3.5-mm externally irrigated-tip quadripolar ablation catheter (ThermoCool, Biosense Webster) with a power of up to 35 W, a target temperature of r381C, and an irrigation rate of 30 mL/min. The power was limited to 20 W on the posterior wall close to the esophagus. After completing PVAI, a 30 mg bolus of adenosine triphosphate was injected with isoproterenol to unmask any dormant PV conduction, and any gaps
1561 responsible for dormant conduction were eliminated by additional RF application(s) until no further dormant conduction could be exposed by repeat adenosine test(s).17,18 In patients with nonparoxysmal AF, substrate modification, when AF persisted after PVAI, was performed sequentially to eliminate complex fractionated atrial electrograms in both atria. The end point of substrate ablation was termination of AF and restoration of sinus rhythm by ablation. If AF continued after substrate ablation, patients underwent internal electrical cardioversion. No antiarrhythmic drugs were given during the procedure. If AF converted to an atrial tachycardia, it was mapped and ablated using 3-dimensional activation mapping and entrainment maneuvers.19 When a critical isthmus of a macroreentrant circuit was identified, lesions were deployed to achieve complete bidirectional conduction block. The cavotricuspid isthmus (CTI) was also ablated to create bidirectional conduction block if a typical common atrial flutter (AFL) morphology was detected on the 12-lead electrogram or identified during the ablation procedure.20 No induction test was performed during the index procedure.
SVC isolation The arrhythmogenicity of the SVC was confirmed using a circular mapping catheter placed in the SVC if it was suspected during the procedure (Figure 1). When the arrhythmogenicity was proven, electrical SVC isolation was performed during pacing from the high RA. The circular mapping catheter was placed at the level of the lower border of the pulmonary artery above the SVC-RA junction guided by SVC angiography. RF energy was delivered point by point for 30 seconds at each point using a 4-mm-tip nonirrigated catheter in a temperature-controlled mode with the maximum temperature set at 501C and the maximum power at 35 W. Before the RF delivery, high-output pacing (10 mA) was performed. If diaphragmatic stimulation was observed, sites without phrenic nerve capture were searched whenever possible. After January 2012, RF energy was applied at the sites regardless of phrenic nerve capture with a maximum power of 10 W.21 The end point of ablation was the elimination of all SVC potentials on the mapping catheter.
Repeat procedure In patients with clinical recurrence of atrial tachyarrhythmia (ATa), a repeat procedure was undertaken. At the outset, PVs were checked with a circumferential catheter. In the case of PV reconduction, additional RF applications were performed to reisolate it. Then, a pacing protocol was undertaken to identify non-PV triggers during isoproterenol infusion. Cardioversion of sustained AF was undertaken.
Follow-up Patients underwent continuous, in-hospital ECG monitoring for 2–4 days after the procedure. The first outpatient clinic visit was 3 weeks after the ablation procedure. Subsequent
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Figure 1 A: A representative case. A circular mapping catheter was placed in the SVC. AF initiation from the SVC (asterisk) was identified. B: Another case. Rapid activity was observed in the SVC during AF. AF converted to sinus rhythm (asterisk) when electrical SVC isolation was achieved despite sustained rapid SVC activity. AF ¼ atrial fibrillation; CS ¼ coronary sinus; d ¼ distal; HRA ¼ high right atrium; p ¼ proximal; SVC ¼ superior vena cava.
follow-up visits consisted of clinical interview, ECGs, and 24-hour Holter monitoring every 3 months at our cardiology clinic. No antiarrhythmic drugs were prescribed after a 3month blanking period. Patients with palpitations were encouraged to use an event recorder. For the detection of any asymptomatic events, we used an external loop recorder (SpiderFlash, Sorin, France),22 which enabled the automatic detection of any ATa for 14 consecutive days. Recurrence was defined according to the patient’s symptoms and/or if an arrhythmia lasting longer than 30 seconds was documented. A repeat procedure was strongly recommended for patients with documented recurrent ATa.
Statistical analysis Continuous data are expressed as mean ⫾ SD for normally distributed variables and as median (25th–75th percentiles) for nonnormally distributed variables, and the data were
compared using a Student t test or Mann-Whitney U test, respectively. Categorical variables were compared by using a χ2 test. A multiple logistic regression analysis was used to determine the predictors of an arrhythmogenic SVC. Variables whose univariate analyses had a P value of o.05 were included in the multiple logistic regression model. A P value of o.05 indicated statistical significance.
Results Prevalence of arrhythmogenic SVCs Of the 836 patients, 61 (7.3%), 2 (0.3%), 3 (0.4%), 2 (0.3%), 1 (0.1%), and 1 (0.1%) patients had a left common PV, inferior common PV, persistent left SVC, false tendon in the LA, dexiocardia, or remnant of the left inferior PV after lobectomy, respectively. No other anatomical deformities were observed in either the atrium or the thoracic veins on
Miyazaki et al Table 1
Predictors of an Arrhythmogenic SVC
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Clinical characteristics of patients with an a-SVC and those without an a-SVC
Characteristic
Patients with an a-SVC
Patients without an a-SVC
P
No. of patients Age (y) Gender: female Paroxysmal AF Duration of AF (y) Structural heart disease Hypertension Body mass index (kg/m2) LA diameter (mm) LV ejection fraction (%) LV diastolic diameter (mm) Coexistence of spontaneous AFL Anatomical deformities SVC diameter (mm) Substrate modification
44 58.5 ⫾ 10.5 13 (30.0) 39 (88.6) 5.0 (2.0–8.5) 1 (2.3) 12 (27.3) 23.5 ⫾ 3.7 38.5 ⫾ 5.7 66.0 ⫾ 5.5 45.9 ⫾ 5.3 19 (43.2) 2 (4.6) 16.6 ⫾ 3.3 3 (6.8)
792 62.5 ⫾ 10.4 191 (24.1) 481 (60.7) 4.5 (2.0–6.5) 124 (15.7) 322 (40.7) 24.6 ⫾ 3.7 42.6 ⫾ 6.3 64.1 ⫾ 9.0 46.5 ⫾ 5.5 186 (23.5) 68 (8.6) 17.3 ⫾ 3.1 235 (29.7)
.015 .414 .0008 .180 .015 .078 .047 .0001 .204 .636 .003 .346 .483 .001
Values are presented as mean ⫾ SD, as median (25th–75th percentiles), or as n (%). AF ¼ atrial fibrillation; AFL ¼ atrial flutter; a-SVC ¼ arrhythmogenic superior vena cava; LA ¼ left atrial; LV ¼ left ventricular; SVC ¼ superior vena cava.
the preprocedural cardiac computed tomography. Successful PVAI was achieved in all patients during the index procedure. An arrhythmogenic SVC was identified in 44 patients (5.3%) during a total of 1063 procedures (1.3 procedures per patient). It was identified during the first, second, and third procedures in 33, 9, and 2 patients, respectively. In 25 patients (56.8%), it was identified spontaneously or with isoproterenol infusion during the procedure. In 13 patients (29.5%) and 6 patients (13.6%), respectively, it was identified by an adenosine injection and after internal cardioversion for sustained AF induced by programmed stimulation or mechanical stimulation. There was no significant difference among the 3 groups in terms of the clinical characteristics. The clinical and echocardiographic characteristics of patients with and without an arrhythmogenic SVC are summarized in Table 1. There was a significant difference in the prevalence of an arrhythmogenic SVC between patients with paroxysmal AF, those with persistent AF, and those with long-standing persistent AF (39 of 520 [7.5%] vs 3 of 158 [1.9%] vs 2 of 158 [1.3%]; P ¼ .0003). In 44 patients with arrhythmogenic SVCs, common AFL was observed before the first procedure in 11 and occurred spontaneously without an induction test during the first procedure in 8. In a total of 19 patients (43.2%), the coexistence of spontaneous AFL was confirmed in the index procedure, whereas it was confirmed in 186 of 792 patients Table 2
without an arrhythmogenic SVC (23.5%; P ¼ .003). Patients with an arrhythmogenic SVC were younger, less obese, and had a smaller LA size than those without an arrhythmogenic SVC. The presence of structural heart disease and hypertension was lower in patients with an arrhythmogenic SVC than in those without. The diameter of the SVC measured by cardiac computed tomography was similar between the 2 groups. A multiple logistic regression analysis revealed that a smaller LA size (odds ratio 0.93; 95% confidence interval 0.88–0.99; P ¼ .038) and coexistence of spontaneous common AFL at the time of the index procedure (odds ratio 2.01; 95% confidence interval 1.00–4.02; P ¼ .048) were the independent predictors for identifying an arrhythmogenic SVC (Table 2). After an adjustment for other clinical variables, each 1-mm decrease in the LA diameter was associated with a 6.8% increase and the coexistence of spontaneous common AFL had a 2.01-fold increase, respectively, in the probability of an arrhythmogenic SVC.
Procedural and clinical outcome An arrhythmogenic SVC was successfully isolated in all 44 patients. In 10 patients (22.7%), a confined SVC tachycardia/ fibrillation was observed after electrical SVC isolation (Figure 1B). No complications were observed except for right phrenic nerve palsy in 2 patients (4.5%) during the procedure, which recovered within a week. Of 44 patients,
Adjusted odds ratio for the predictors for identifying an a-SVC using a logistic regression analysis
Characteristic
P
Odds ratio
95% confidence interval
Age Structural heart disease Body mass index Paroxysmal AF LA diameter Coexistence of spontaneous AFL
.083 .128 .621 .056 .038 .048
0.936 2.01
0.880–0.996 1.004–4.026
AF ¼ atrial fibrillation; AFL ¼ atrial flutter; a-SVC ¼ arrhythmogenic superior vena cava; LA ¼ left atrial.
1564 19 (43.2%) and 6 (13.6%) patients underwent a second and a third ablation procedure for recurrent ATa a median of 13.0 months (25th–75th percentiles 4.0–29.0 months) and 16.0 months (25th–75th percentile 4.5–54.8 months) after the index procedure, respectively. The recurrent arrhythmia was common AFL in 3 patients and AF in the remainder. In 19 patients who underwent a second procedure, an initial SVC isolation and CTI ablation were performed during the second procedure in 8 patients (42.1%) and 6 patients (31.6%), respectively. In 3 patients, common AFL was documented during the second procedure for the first time. In 8 patients who underwent SVC isolation during the index procedure, SVC reconnection was observed in 6 patients (75.0%) including 5 with PV reconnections. In these 6 patients, SVC-associated recurrent ATa were observed during the procedure in 2. In both cases, ATa were provoked by an adenosine injection. Arrhythmogenic PVs were not identified during the index or second procedure in these 6 patients. In 13 patients in whom bidirectional CTI block was created during the index procedure, reconduction was observed in 3 (23.1%). PV reconnections were observed in 17 patients (89.5%) with a median of 2.0 PVs (25th–75th percentiles 1.0–4.0 PVs). All conduction gaps were closed by RF applications during the procedure. In 6 patients who underwent a third procedure, an initial SVC isolation was performed in 3 (50.0%). In these 3 patients who underwent SVC isolation previously (1 patient in the index procedure and 2 in the second procedure), SVC reconnection was observed in all patients including 2 with PV reconnections. In 1 patient, rapid activity was recorded in the SVC during AF, and AF converted to sinus rhythm when the achievement of reisolation despite sustained fibrillation inside the isolated area in the third procedure. Bidirectional CTI block was created during the previous procedure in all 6 patients, and reconduction was observed in 1 (16.7%). PV reconnections of a median of 1.0 PV (25th–75th percentiles 0.75–2.0 PVs) were observed in 5 patients (83.3%). All conduction gaps were closed by RF applications during the procedure. Thirty-nine of 44 patients (88.6%) were free from any ATa without any antiarrhythmic drugs at a median of 16.5 months (25th–75th percentiles 9.0–27.0 months) after a mean of 1.5 ⫾ 0.7 procedures. In total, common AFL was identified in 25 of 44 patients with arrhythmogenic SVCs (56.8%) during the follow-up period.
Discussion Major findings The present study investigated the predictors of an arrhythmogenic SVC, which was defined as an SVC associated with AF, in the context of AF ablation. The arrhythmogenicity was evaluated throughout the ablation procedure in all procedures. We found that (1) a smaller LA size and the presence of spontaneous common AFL at the time of the index procedure were independent predictors of an arrhythmogenic SVC, (2) the fewer the number of commonly known factors of AF progression, the higher the prevalence
Heart Rhythm, Vol 11, No 9, September 2014 of an arrhythmogenic SVC, (3) the SVC was associated not only with paroxysmal AF but rarely also with persistent and long-standing persistent AF, and (4) the anatomical information did not predict the arrhythmogenic SVC.
Preprocedural predictors of an arrhythmogenic SVC Atrial myocardial sleeves extend into the SVC,7 and it has been recognized as one of the common sources of AF.8 Lee et al23 evaluated the predictors of SVC ectopic beats initiating AF by comparing patients with (n ¼ 8) and without (n ¼ 255) SVC ectopic beats initiating AF. The results showed that a female gender was the only predictor. Higuchi et al8 showed that the SVC sleeve is longer in patients with SVC-trigged AF (n ¼ 12) than in those without (n ¼ 48). However, both studies focused only on patients with paroxysmal AF and those with SVC-triggered AF. Moreover, the number of patients with SVC-triggered AF was too small to identify the predictors. We recently showed that the SVC acts not only to trigger AF but also to perpetuate AF.9 The present study evaluated the various preprocedural predictors including the anatomical information to identify an arrhythmogenic SVC (both triggers and perpetuators) in a consecutive large AF population series. The present data demonstrated that patients with arrhythmogenic SVCs were younger and had smaller LAs than those without and that the presence of hypertension and structural heart disease was lower in patients with arrhythmogenic SVCs than those without. It is well known that hypertension, underlying heart disease, and advancing age are independent predictors of AF progression.24–26 Underlying diseases might cause chronic stretch and atrial dilation, which seem to be important stimuli for chronic atrial structural remodeling (cellular hypertrophy, fibroblast proliferation, and tissue fibrosis) that enables the maintenance of AF. Hypertension is the most prevalent risk factor for AF in the general population. LA enlargement is a surrogate measure of chronic elevation in the left ventricular filling pressures and the result of anatomical atrial remodeling. Our data demonstrated that the fewer the number of commonly known predictors of AF progression, the higher the prevalence of an arrhythmogenic SVC. The finding that arrhythmogenic SVCs were more commonly observed in paroxysmal AF than in nonparoxysmal AF was in line with the prior finding that empirical SVC isolation resulted in a better outcome in patients with paroxysmal AF but not in those with nonparoxysmal AF.27 This result suggested that the mechanism of AF with an arrhythmogenic SVC differed from that without an arrhythmogenic SVC and that the process of AF progression might be different in this subset. It seems to be unlikely that AF associated with an SVC leads to LA enlargement.
RA arrhythmias: Common AFL and an arrhythmogenic SVC Although the vast majority of triggers/substrates lie in the LA chamber, the RA chamber also plays an important role in
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AF.28 The present study showed that the coexistence of spontaneous AFL at the time of the index procedure was also an independent predictor of an arrhythmogenic SVC. That information would aid in deciding whether the arrhythmogenicity of the SVC should be carefully investigated by additional induction and drug tests. In addition, among patients without spontaneous AFL at the time of the index procedure, AFL was the recurrent arrhythmia in 3 patients and was documented during the repeat procedure in another 3. In contrast, the SVC anatomical information was not useful for predicting the arrhythmogenicity. A possible explanation is that the anatomical distance between the AFL circuit and the SVC is much shorter than that between the AFL circuit and the LA, and macroreentrant tachycardia is more easily inducible by pacing close to the circuit. It is possible that arrhythmogenic SVCs induced spontaneous AFL because firing from the SVC worked like burst pacing from the high RA, which is close to the circuit of common AFL. In fact, the coexistence of AFL in patients without arrhythmogenic SVCs in the present study was less frequent than the coexistence of AFL in a published study29 in which aggressive pacing maneuvers were performed in the index procedure, because we did not perform any pacing maneuvers in the index procedure. Alternatively, the arrhythmogenic and anisotropic substrate properties of the RA resulting from remodeling might contribute to the high incidence of AFL. A previous prospective randomized study pointed out the possible relationship between AFL and non-PV triggers in patients with AF.30 That is, the arrhythmia recurrence rate is higher after PV isolation and CTI ablation in patients with paroxysmal AF (PAF)/AFL than that after PV isolation alone in patients with AF and no documented common AFL.
Clinical implications Although electrical isolation is an established therapy for arrhythmogenic SVCs,10 it is troublesome to identify the arrhythmogenicity in empirical AF ablation procedures.11 The study data provide clues to consider arrhythmogenic SVCs. First, the possibility of an arrhythmogenic SVC should be kept in mind in patients with paroxysmal AF having small LAs. Second, if spontaneous common AFL is observed before or during the index procedure, the arrhythmogenicity of the SVC should be evaluated using drug and induction tests. Third, if arrhythmogenic SVCs are identified during the procedure, an AFL induction test should be performed to evaluate the coexistence because 3/25 (12%) of the patients without spontaneous AFL at the time of the index procedure had recurrent AFL during the follow-up period and 25/44 (56.8%) of the patients with arrhythmogenic SVCs had coexisting AFL.
Study limitations The length of the SVC sleeve was not evaluated in the present study.
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Conclusion A smaller LA size and the coexistence of spontaneous common AFL were independent predictors of an arrhythmogenic SVC in the context of AF ablation.
Acknowledgments We thank Mr John Martin for extending his assistance in the preparation of this manuscript.
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radiofrequency catheter ablation. J Cardiovasc Electrophysiol 2004;15: 1041–1047. Hachiya H, Hirao K, Takahashi A, Nagata Y, Suzuki K, Maeda S, Sasaki T, Kawabata M, Isobe M, Iesaka Y. Clinical implications of reconnection between the left atrium and isolated pulmonary veins provoked by adenosine triphosphate after extensive encircling pulmonary vein isolation. J Cardiovasc Electrophysiol 2007;18:1–7. Jaïs P, Matsuo S, Knecht S, Weerasooriya R, Hocini M, Sacher F, Wright M, Nault I, Lellouche N, Klein G, Clémenty J, Haïssaguerre M. A deductive mapping strategy for atrial tachycardia following atrial fibrillation ablation: importance of localized reentry. J Cardiovasc Electrophysiol 2009;20:480–491. Shah D, Haïssaguerre M, Takahashi A, Jaïs P, Hocini M, Clémenty J. Differential pacing for distinguishing block from persistent conduction through an ablation line. Circulation 2000;102:1517–1522. Sacher F, Monahan KH, Thomas SP, et al. Phrenic nerve injury after atrial fibrillation catheter ablation: characterization and outcome in a multicenter study. J Am Coll Cardiol 2006;47:2498–2503. Locati ET, Vecchi AM, Vargiu S, Cattafi G, Lunati M. Role of extended external loop recorders for the diagnosis of unexplained syncope, pre-syncope, and sustained palpitations. Europace 2014;16:914–922. Lee SH, Tai CT, Hsieh MH, Tsao HM, Lin YJ, Chang SL, Huang JL, Lee KT, Chen YJ, Cheng JJ, Chen SA. Predictors of non-pulmonary vein ectopic beats initiating paroxysmal atrial fibrillation: implication for catheter ablation. J Am Coll Cardiol 2005;46:1054–1059.
Heart Rhythm, Vol 11, No 9, September 2014 24. Kerr CR, Humphries KH, Talajic M, Klein GJ, Connolly SJ, Green M, Boone J, Sheldon R, Dorian P, Newman D. Progression to chronic atrial fibrillation after the initial diagnosis of paroxysmal atrial fibrillation: results from the Canadian Registry of Atrial Fibrillation. Am Heart J 2005;149:489–496. 25. de Vos CB, Pisters R, Nieuwlaat R, Prins MH, Tieleman RG, Coelen RJ, van den Heijkant AC, Allessie MA, Crijns HJ. Progression from paroxysmal to persistent atrial fibrillation clinical correlates and prognosis. J Am Coll Cardiol 2010;55:725–731. 26. Psaty BM, Manolio TA, Kuller LH, Kronmal RA, Cushman M, Fried LP, White R, Furberg CD, Rautaharju PM. Incidence of and risk factors for atrial fibrillation in older adults. Circulation 1997;96:2455–2461. 27. Arruda M, Mlcochova H, Prasad SK, et al. Electrical isolation of the superior vena cava: an adjunctive strategy to pulmonary vein antrum isolation improving the outcome of AF ablation. J Cardiovasc Electrophysiol 2007;18:1261–1266. 28. Hocini M, Nault I, Wright M, et al. Disparate evolution of right and left atrial rate during ablation of long-lasting persistent atrial fibrillation. J Am Coll Cardiol 2010;55:1007–1016. 29. Shah DC, Sunthorn H, Burri H, Gentil-Baron P. Evaluation of an individualized strategy of cavotricuspid isthmus ablation as an adjunct to atrial fibrillation ablation. J Cardiovasc Electrophysiol 2007;18:926–930. 30. Moreira W, Timmermans C, Wellens HJ, Mizusawa Y, Philippens S, Perez D, Rodriguez LM. Can common-type atrial flutter be a sign of an arrhythmogenic substrate in paroxysmal atrial fibrillation? Clinical and ablative consequences in patients with coexistent paroxysmal atrial fibrillation/atrial flutter. Circulation 2007;116:2786–2792.
Introduction Recognition and targeting of pulmonary vein (PV) triggers have led to a dramatic rise in the efficacy and prominence of atrial fibrillation (AF) catheter ablation.1–3 Despite the critical role of the PVs and PV antrum in AF,3–5 non-PV foci have also been established as important sources of AF.6 The superior vena cava (SVC), one of the thoracic veins, contains atrial muscle sleeves extending up to a short distance from the right atrium (RA)7 and acts not only as a trigger but also as a driver of AF like the PVs.8,9 Although electrical isolation has been the established strategy for arrhythmogenic SVCs,10 the identification is not always easy and missing the arrhythmogenicity leads to an arrhythmia recurrence after the ablation procedure. In fact, in some of the cases, the arrhythmogenicity is identified in a repeat procedure and various provocative maneuvers are required to Address reprint requests and correspondence: Dr Shinsuke Miyazaki, Cardiology Division, Cardiovascular Center, Tsuchiura Kyodo Hospital, 11-7 Manabeshin-machi, Tsuchiura, Ibaraki 300-0053, Japan. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
spontaneous common AFL (odds ratio 2.01; 95% confidence interval 1.00–4.02; P ¼ .048) were independent predictors identifying an aSVC. Although 19 patients (43.2%) required repeat procedures, 39 (88.6%) were free from any atrial tachyarrhythmias without antiarrhythmic drugs at a median of 16.5 months (25th–75th percentiles 9.0–27.0 months) after a mean of 1.5 ⫾ 0.7 procedures. CONCLUSION A smaller LA size and coexistence of spontaneous common AFL were independent predictors of an a-SVC in the context of AF ablation. KEYWORDS Superior vena cava; Arrhythmogenicity; fibrillation; Predictor; Catheter ablation
Atrial
ABBREVIATIONS AF ¼ atrial fibrillation; AFL ¼ atrial flutter; ATa ¼ atrial tachyarrhythmia; CTI ¼ cavotricuspid isthmus; ECG ¼ electrocardiogram/electrocardiographic; LA ¼ left atrium/atrial; PV ¼ pulmonary vein; PVAI ¼ pulmonary vein antrum isolation; RA ¼ right atrium; RF ¼ radiofrequency; SVC ¼ superior vena cava (Heart Rhythm 2014;11:1560–1566) I 2014 Heart Rhythm Society. All rights reserved.
find it out.11 Thus, knowing the predictors of arrhythmogenic SVCs would be helpful in the context of AF ablation. The objective of this study was to elucidate the predictors of arrhythmogenic SVCs (triggers and perpetuators of AF) in the context of AF ablation.
Methods Study population This study consisted of 836 consecutive patients who underwent catheter ablation of drug-resistant AF between April 2010 and December 2013 at our institute. The arrhythmogenicity of the SVC was evaluated with a mapping catheter throughout the ablation procedure in all procedures. All patients underwent pulmonary vein antrum isolation (PVAI) in the index procedure. An additional SVC isolation was undertaken for arrhythmogenic SVCs whenever the arrhythmogenicity was identified. An arrhythmogenic SVC was defined as an SVC triggering AF and an SVC associated with the maintenance of AF.9 Solitary premature atrial contractions without AF originating from the SVC did not define an arrhythmogenic SVC in this study. AF was http://dx.doi.org/10.1016/j.hrthm.2014.06.016
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classified according to the 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of AF. All patients gave their written informed consent for participation in the study.12
Mapping and ablation protocol All antiarrhythmic drugs were discontinued for at least 5 half-lives before the procedure. All patients were effectively anticoagulated for 41 month before the procedure. Transesophageal echocardiography was performed to exclude any atrial thrombi. The surface electrocardiogram (ECG) and bipolar intracardiac electrograms were continuously monitored and stored on a computer-based digital recording system (LabSystem PRO, Bard Electrophysiology, Lowell, MA). The bipolar electrograms were filtered from 30 to 500 Hz. A 7-F 14-pole 2-site mapping catheter (Irvine Biomedical Inc, Irvin, CA) or a 7-F 20-pole 3-site mapping catheter (BeeAT, Japan Life Line, Tokyo, Japan) was inserted through the right jugular vein. The proximal poles were positioned at the SVC-RA junction and distal poles in the coronary sinus for pacing, continuous recording, and internal AF cardioversion during the entire procedure. The proximal electrodes enabled continuous monitoring of the SVC during the entire procedure. The electrophysiology study was performed under mild sedation obtained with pentazocine and hydroxyzine pamoate.
Ablation procedure Ablation was performed according to the strategy described previously.13–15 In brief, after a single transseptal puncture, 2 long sheaths (SL0, St Jude Medical, Minneapolis, MN) were introduced into both superior PVs. Pulmonary venography during ventricular pacing and contrast esophagography were performed to obtain the relative locations of the PV ostia vis-à-vis esophagus. A 100 IU/kg body weight dose of heparin was administered after the transseptal puncture, and heparinized saline was also infused to maintain the activated clotting time at 250–350 seconds. Two circular mapping catheters (Lasso, Biosense Webster, Diamond Bar, CA) were placed in the superior and inferior PVs, and the left- and right-sided ipsilateral PVs were circumferentially and extensively ablated guided by a 3-dimensional mapping system (CARTO 3, Biosense Webster). Posteriorly, ablation was performed anatomically in the left atrium (LA), 1–3 cm from the PV ostia. Anteriorly, ablation was performed on the edge of the left PVs guided by the earliest PV potentials. The end point was achievement of bidirectional conduction block between the LA and PVs.16 Radiofrequency (RF) current was delivered point by point with a 3.5-mm externally irrigated-tip quadripolar ablation catheter (ThermoCool, Biosense Webster) with a power of up to 35 W, a target temperature of r381C, and an irrigation rate of 30 mL/min. The power was limited to 20 W on the posterior wall close to the esophagus. After completing PVAI, a 30 mg bolus of adenosine triphosphate was injected with isoproterenol to unmask any dormant PV conduction, and any gaps
1561 responsible for dormant conduction were eliminated by additional RF application(s) until no further dormant conduction could be exposed by repeat adenosine test(s).17,18 In patients with nonparoxysmal AF, substrate modification, when AF persisted after PVAI, was performed sequentially to eliminate complex fractionated atrial electrograms in both atria. The end point of substrate ablation was termination of AF and restoration of sinus rhythm by ablation. If AF continued after substrate ablation, patients underwent internal electrical cardioversion. No antiarrhythmic drugs were given during the procedure. If AF converted to an atrial tachycardia, it was mapped and ablated using 3-dimensional activation mapping and entrainment maneuvers.19 When a critical isthmus of a macroreentrant circuit was identified, lesions were deployed to achieve complete bidirectional conduction block. The cavotricuspid isthmus (CTI) was also ablated to create bidirectional conduction block if a typical common atrial flutter (AFL) morphology was detected on the 12-lead electrogram or identified during the ablation procedure.20 No induction test was performed during the index procedure.
SVC isolation The arrhythmogenicity of the SVC was confirmed using a circular mapping catheter placed in the SVC if it was suspected during the procedure (Figure 1). When the arrhythmogenicity was proven, electrical SVC isolation was performed during pacing from the high RA. The circular mapping catheter was placed at the level of the lower border of the pulmonary artery above the SVC-RA junction guided by SVC angiography. RF energy was delivered point by point for 30 seconds at each point using a 4-mm-tip nonirrigated catheter in a temperature-controlled mode with the maximum temperature set at 501C and the maximum power at 35 W. Before the RF delivery, high-output pacing (10 mA) was performed. If diaphragmatic stimulation was observed, sites without phrenic nerve capture were searched whenever possible. After January 2012, RF energy was applied at the sites regardless of phrenic nerve capture with a maximum power of 10 W.21 The end point of ablation was the elimination of all SVC potentials on the mapping catheter.
Repeat procedure In patients with clinical recurrence of atrial tachyarrhythmia (ATa), a repeat procedure was undertaken. At the outset, PVs were checked with a circumferential catheter. In the case of PV reconduction, additional RF applications were performed to reisolate it. Then, a pacing protocol was undertaken to identify non-PV triggers during isoproterenol infusion. Cardioversion of sustained AF was undertaken.
Follow-up Patients underwent continuous, in-hospital ECG monitoring for 2–4 days after the procedure. The first outpatient clinic visit was 3 weeks after the ablation procedure. Subsequent
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Figure 1 A: A representative case. A circular mapping catheter was placed in the SVC. AF initiation from the SVC (asterisk) was identified. B: Another case. Rapid activity was observed in the SVC during AF. AF converted to sinus rhythm (asterisk) when electrical SVC isolation was achieved despite sustained rapid SVC activity. AF ¼ atrial fibrillation; CS ¼ coronary sinus; d ¼ distal; HRA ¼ high right atrium; p ¼ proximal; SVC ¼ superior vena cava.
follow-up visits consisted of clinical interview, ECGs, and 24-hour Holter monitoring every 3 months at our cardiology clinic. No antiarrhythmic drugs were prescribed after a 3month blanking period. Patients with palpitations were encouraged to use an event recorder. For the detection of any asymptomatic events, we used an external loop recorder (SpiderFlash, Sorin, France),22 which enabled the automatic detection of any ATa for 14 consecutive days. Recurrence was defined according to the patient’s symptoms and/or if an arrhythmia lasting longer than 30 seconds was documented. A repeat procedure was strongly recommended for patients with documented recurrent ATa.
Statistical analysis Continuous data are expressed as mean ⫾ SD for normally distributed variables and as median (25th–75th percentiles) for nonnormally distributed variables, and the data were
compared using a Student t test or Mann-Whitney U test, respectively. Categorical variables were compared by using a χ2 test. A multiple logistic regression analysis was used to determine the predictors of an arrhythmogenic SVC. Variables whose univariate analyses had a P value of o.05 were included in the multiple logistic regression model. A P value of o.05 indicated statistical significance.
Results Prevalence of arrhythmogenic SVCs Of the 836 patients, 61 (7.3%), 2 (0.3%), 3 (0.4%), 2 (0.3%), 1 (0.1%), and 1 (0.1%) patients had a left common PV, inferior common PV, persistent left SVC, false tendon in the LA, dexiocardia, or remnant of the left inferior PV after lobectomy, respectively. No other anatomical deformities were observed in either the atrium or the thoracic veins on
Miyazaki et al Table 1
Predictors of an Arrhythmogenic SVC
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Clinical characteristics of patients with an a-SVC and those without an a-SVC
Characteristic
Patients with an a-SVC
Patients without an a-SVC
P
No. of patients Age (y) Gender: female Paroxysmal AF Duration of AF (y) Structural heart disease Hypertension Body mass index (kg/m2) LA diameter (mm) LV ejection fraction (%) LV diastolic diameter (mm) Coexistence of spontaneous AFL Anatomical deformities SVC diameter (mm) Substrate modification
44 58.5 ⫾ 10.5 13 (30.0) 39 (88.6) 5.0 (2.0–8.5) 1 (2.3) 12 (27.3) 23.5 ⫾ 3.7 38.5 ⫾ 5.7 66.0 ⫾ 5.5 45.9 ⫾ 5.3 19 (43.2) 2 (4.6) 16.6 ⫾ 3.3 3 (6.8)
792 62.5 ⫾ 10.4 191 (24.1) 481 (60.7) 4.5 (2.0–6.5) 124 (15.7) 322 (40.7) 24.6 ⫾ 3.7 42.6 ⫾ 6.3 64.1 ⫾ 9.0 46.5 ⫾ 5.5 186 (23.5) 68 (8.6) 17.3 ⫾ 3.1 235 (29.7)
.015 .414 .0008 .180 .015 .078 .047 .0001 .204 .636 .003 .346 .483 .001
Values are presented as mean ⫾ SD, as median (25th–75th percentiles), or as n (%). AF ¼ atrial fibrillation; AFL ¼ atrial flutter; a-SVC ¼ arrhythmogenic superior vena cava; LA ¼ left atrial; LV ¼ left ventricular; SVC ¼ superior vena cava.
the preprocedural cardiac computed tomography. Successful PVAI was achieved in all patients during the index procedure. An arrhythmogenic SVC was identified in 44 patients (5.3%) during a total of 1063 procedures (1.3 procedures per patient). It was identified during the first, second, and third procedures in 33, 9, and 2 patients, respectively. In 25 patients (56.8%), it was identified spontaneously or with isoproterenol infusion during the procedure. In 13 patients (29.5%) and 6 patients (13.6%), respectively, it was identified by an adenosine injection and after internal cardioversion for sustained AF induced by programmed stimulation or mechanical stimulation. There was no significant difference among the 3 groups in terms of the clinical characteristics. The clinical and echocardiographic characteristics of patients with and without an arrhythmogenic SVC are summarized in Table 1. There was a significant difference in the prevalence of an arrhythmogenic SVC between patients with paroxysmal AF, those with persistent AF, and those with long-standing persistent AF (39 of 520 [7.5%] vs 3 of 158 [1.9%] vs 2 of 158 [1.3%]; P ¼ .0003). In 44 patients with arrhythmogenic SVCs, common AFL was observed before the first procedure in 11 and occurred spontaneously without an induction test during the first procedure in 8. In a total of 19 patients (43.2%), the coexistence of spontaneous AFL was confirmed in the index procedure, whereas it was confirmed in 186 of 792 patients Table 2
without an arrhythmogenic SVC (23.5%; P ¼ .003). Patients with an arrhythmogenic SVC were younger, less obese, and had a smaller LA size than those without an arrhythmogenic SVC. The presence of structural heart disease and hypertension was lower in patients with an arrhythmogenic SVC than in those without. The diameter of the SVC measured by cardiac computed tomography was similar between the 2 groups. A multiple logistic regression analysis revealed that a smaller LA size (odds ratio 0.93; 95% confidence interval 0.88–0.99; P ¼ .038) and coexistence of spontaneous common AFL at the time of the index procedure (odds ratio 2.01; 95% confidence interval 1.00–4.02; P ¼ .048) were the independent predictors for identifying an arrhythmogenic SVC (Table 2). After an adjustment for other clinical variables, each 1-mm decrease in the LA diameter was associated with a 6.8% increase and the coexistence of spontaneous common AFL had a 2.01-fold increase, respectively, in the probability of an arrhythmogenic SVC.
Procedural and clinical outcome An arrhythmogenic SVC was successfully isolated in all 44 patients. In 10 patients (22.7%), a confined SVC tachycardia/ fibrillation was observed after electrical SVC isolation (Figure 1B). No complications were observed except for right phrenic nerve palsy in 2 patients (4.5%) during the procedure, which recovered within a week. Of 44 patients,
Adjusted odds ratio for the predictors for identifying an a-SVC using a logistic regression analysis
Characteristic
P
Odds ratio
95% confidence interval
Age Structural heart disease Body mass index Paroxysmal AF LA diameter Coexistence of spontaneous AFL
.083 .128 .621 .056 .038 .048
0.936 2.01
0.880–0.996 1.004–4.026
AF ¼ atrial fibrillation; AFL ¼ atrial flutter; a-SVC ¼ arrhythmogenic superior vena cava; LA ¼ left atrial.
1564 19 (43.2%) and 6 (13.6%) patients underwent a second and a third ablation procedure for recurrent ATa a median of 13.0 months (25th–75th percentiles 4.0–29.0 months) and 16.0 months (25th–75th percentile 4.5–54.8 months) after the index procedure, respectively. The recurrent arrhythmia was common AFL in 3 patients and AF in the remainder. In 19 patients who underwent a second procedure, an initial SVC isolation and CTI ablation were performed during the second procedure in 8 patients (42.1%) and 6 patients (31.6%), respectively. In 3 patients, common AFL was documented during the second procedure for the first time. In 8 patients who underwent SVC isolation during the index procedure, SVC reconnection was observed in 6 patients (75.0%) including 5 with PV reconnections. In these 6 patients, SVC-associated recurrent ATa were observed during the procedure in 2. In both cases, ATa were provoked by an adenosine injection. Arrhythmogenic PVs were not identified during the index or second procedure in these 6 patients. In 13 patients in whom bidirectional CTI block was created during the index procedure, reconduction was observed in 3 (23.1%). PV reconnections were observed in 17 patients (89.5%) with a median of 2.0 PVs (25th–75th percentiles 1.0–4.0 PVs). All conduction gaps were closed by RF applications during the procedure. In 6 patients who underwent a third procedure, an initial SVC isolation was performed in 3 (50.0%). In these 3 patients who underwent SVC isolation previously (1 patient in the index procedure and 2 in the second procedure), SVC reconnection was observed in all patients including 2 with PV reconnections. In 1 patient, rapid activity was recorded in the SVC during AF, and AF converted to sinus rhythm when the achievement of reisolation despite sustained fibrillation inside the isolated area in the third procedure. Bidirectional CTI block was created during the previous procedure in all 6 patients, and reconduction was observed in 1 (16.7%). PV reconnections of a median of 1.0 PV (25th–75th percentiles 0.75–2.0 PVs) were observed in 5 patients (83.3%). All conduction gaps were closed by RF applications during the procedure. Thirty-nine of 44 patients (88.6%) were free from any ATa without any antiarrhythmic drugs at a median of 16.5 months (25th–75th percentiles 9.0–27.0 months) after a mean of 1.5 ⫾ 0.7 procedures. In total, common AFL was identified in 25 of 44 patients with arrhythmogenic SVCs (56.8%) during the follow-up period.
Discussion Major findings The present study investigated the predictors of an arrhythmogenic SVC, which was defined as an SVC associated with AF, in the context of AF ablation. The arrhythmogenicity was evaluated throughout the ablation procedure in all procedures. We found that (1) a smaller LA size and the presence of spontaneous common AFL at the time of the index procedure were independent predictors of an arrhythmogenic SVC, (2) the fewer the number of commonly known factors of AF progression, the higher the prevalence
Heart Rhythm, Vol 11, No 9, September 2014 of an arrhythmogenic SVC, (3) the SVC was associated not only with paroxysmal AF but rarely also with persistent and long-standing persistent AF, and (4) the anatomical information did not predict the arrhythmogenic SVC.
Preprocedural predictors of an arrhythmogenic SVC Atrial myocardial sleeves extend into the SVC,7 and it has been recognized as one of the common sources of AF.8 Lee et al23 evaluated the predictors of SVC ectopic beats initiating AF by comparing patients with (n ¼ 8) and without (n ¼ 255) SVC ectopic beats initiating AF. The results showed that a female gender was the only predictor. Higuchi et al8 showed that the SVC sleeve is longer in patients with SVC-trigged AF (n ¼ 12) than in those without (n ¼ 48). However, both studies focused only on patients with paroxysmal AF and those with SVC-triggered AF. Moreover, the number of patients with SVC-triggered AF was too small to identify the predictors. We recently showed that the SVC acts not only to trigger AF but also to perpetuate AF.9 The present study evaluated the various preprocedural predictors including the anatomical information to identify an arrhythmogenic SVC (both triggers and perpetuators) in a consecutive large AF population series. The present data demonstrated that patients with arrhythmogenic SVCs were younger and had smaller LAs than those without and that the presence of hypertension and structural heart disease was lower in patients with arrhythmogenic SVCs than those without. It is well known that hypertension, underlying heart disease, and advancing age are independent predictors of AF progression.24–26 Underlying diseases might cause chronic stretch and atrial dilation, which seem to be important stimuli for chronic atrial structural remodeling (cellular hypertrophy, fibroblast proliferation, and tissue fibrosis) that enables the maintenance of AF. Hypertension is the most prevalent risk factor for AF in the general population. LA enlargement is a surrogate measure of chronic elevation in the left ventricular filling pressures and the result of anatomical atrial remodeling. Our data demonstrated that the fewer the number of commonly known predictors of AF progression, the higher the prevalence of an arrhythmogenic SVC. The finding that arrhythmogenic SVCs were more commonly observed in paroxysmal AF than in nonparoxysmal AF was in line with the prior finding that empirical SVC isolation resulted in a better outcome in patients with paroxysmal AF but not in those with nonparoxysmal AF.27 This result suggested that the mechanism of AF with an arrhythmogenic SVC differed from that without an arrhythmogenic SVC and that the process of AF progression might be different in this subset. It seems to be unlikely that AF associated with an SVC leads to LA enlargement.
RA arrhythmias: Common AFL and an arrhythmogenic SVC Although the vast majority of triggers/substrates lie in the LA chamber, the RA chamber also plays an important role in
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AF.28 The present study showed that the coexistence of spontaneous AFL at the time of the index procedure was also an independent predictor of an arrhythmogenic SVC. That information would aid in deciding whether the arrhythmogenicity of the SVC should be carefully investigated by additional induction and drug tests. In addition, among patients without spontaneous AFL at the time of the index procedure, AFL was the recurrent arrhythmia in 3 patients and was documented during the repeat procedure in another 3. In contrast, the SVC anatomical information was not useful for predicting the arrhythmogenicity. A possible explanation is that the anatomical distance between the AFL circuit and the SVC is much shorter than that between the AFL circuit and the LA, and macroreentrant tachycardia is more easily inducible by pacing close to the circuit. It is possible that arrhythmogenic SVCs induced spontaneous AFL because firing from the SVC worked like burst pacing from the high RA, which is close to the circuit of common AFL. In fact, the coexistence of AFL in patients without arrhythmogenic SVCs in the present study was less frequent than the coexistence of AFL in a published study29 in which aggressive pacing maneuvers were performed in the index procedure, because we did not perform any pacing maneuvers in the index procedure. Alternatively, the arrhythmogenic and anisotropic substrate properties of the RA resulting from remodeling might contribute to the high incidence of AFL. A previous prospective randomized study pointed out the possible relationship between AFL and non-PV triggers in patients with AF.30 That is, the arrhythmia recurrence rate is higher after PV isolation and CTI ablation in patients with paroxysmal AF (PAF)/AFL than that after PV isolation alone in patients with AF and no documented common AFL.
Clinical implications Although electrical isolation is an established therapy for arrhythmogenic SVCs,10 it is troublesome to identify the arrhythmogenicity in empirical AF ablation procedures.11 The study data provide clues to consider arrhythmogenic SVCs. First, the possibility of an arrhythmogenic SVC should be kept in mind in patients with paroxysmal AF having small LAs. Second, if spontaneous common AFL is observed before or during the index procedure, the arrhythmogenicity of the SVC should be evaluated using drug and induction tests. Third, if arrhythmogenic SVCs are identified during the procedure, an AFL induction test should be performed to evaluate the coexistence because 3/25 (12%) of the patients without spontaneous AFL at the time of the index procedure had recurrent AFL during the follow-up period and 25/44 (56.8%) of the patients with arrhythmogenic SVCs had coexisting AFL.
Study limitations The length of the SVC sleeve was not evaluated in the present study.
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Conclusion A smaller LA size and the coexistence of spontaneous common AFL were independent predictors of an arrhythmogenic SVC in the context of AF ablation.
Acknowledgments We thank Mr John Martin for extending his assistance in the preparation of this manuscript.
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